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Dermatology Board Prep > DERM (03) Papulosquamous Disease > Other papulosquamous dz > Flashcards

Other papulosquamous dz Flashcards

1
Q

What cells are involved in small plaque parapsoriasis?

A

CD4+ T cells

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2
Q

What is the estimated progression from large plaque parapsorasis to MF

A

10-35%

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3
Q

What are the differences in T-cells in PLEVA vs PLC?

A

CD8+ in PLEVA and CD4+ in PLC

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4
Q

Clinical presentation of PLEVA?

A

Rapid onset of widespread (trunk, buttocks, proximal extremities) pink papules, evolve into vesicular ulceronecrtoic purpuric and cursted papuels.

Heals with varioliform scars after weeks

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5
Q

Clinical of PLC?

A

widespread scaly red-brown papules and plaques. Resolves w/ hypopigmentation after weeks to months

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6
Q

What clinical feature can predict the length to resolution for PLC?

A

More widespread = shorter time to resolution. Less widespread = longer

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7
Q

Pneumonic for PLEVA path?

A

Parakeratosis Lichenoid infiltrate Extrravased RBC V-shaped dermal lymphocytic infilate Acute epidermal changes (dyskeratosis, ulceration, neutrophilic scale crust) CD8

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8
Q

What cell should you not see in PLEVA or PLC on path?

A

Eos!

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9
Q

Age distribution of PRP?

A

Bimodal: 1st and 6th decade

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10
Q

First sign of PRP?

A

Folliculocentric keratotic papules on erythematous base (nutmeg-grater)

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11
Q

Other clinical features of PRP?

A

Scalp erythema, diffuse scaling, folliculocentric keratotic papules on erythematous base, orange-red waxy keratoderma of palms soles, rash spreads caudally

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12
Q

What type of PRP is most common in kids?

A

Type IV or circumscribed juvenile

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13
Q

What form of PRP is inherited/familial?

A

V/atypical juvenile

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14
Q

Clinical findings in PRP a/w HIV?

A

follicular spines, acne conglobata, hidradenitis suppurativa

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15
Q

Epi of Pityriasis rosea?

A

adolescents and young adults

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16
Q

Christmas tree ddx?

A

PR, KS, secondary syphillis, SK, parapsoriasis/mycosis fungoides, lichen planus pigmentosus/ashy dermatosis

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17
Q

What causes PR?

A

HHV-7 and HHV-6 commonily

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18
Q

Drugs a/w PR?

A

ACEI, gold, B-blocker are the big ones. Also NSAIDS, bismuth, barbiturates, isotretinon, metronidazole, clonidine

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19
Q

Natural course of PR?

A

goes away spontaneously over 6-8 weeks

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20
Q

What is the VIDAL type of PR?

A

Recurrent or persistent PR

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21
Q

What medication can shorten the dz course in PR?

A

Erythromycin

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22
Q

PR issues in pregnancies?

A

There is an association as a report of a possible risk of sponateous abortion

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23
Q

Etiology of granular parakeratosis?

A

defect in filaggrin meatbolism –> retention of keratohyaline granules in stratum corneum.

24
Q

What defines small plaque vs large plaque parasporasis?

A

small plaque = <5cm in diameter large plaque = >5cm in diameter

25
Q

Clinical presentation of parapsoriasis?

A

Chronic, usually asymptomatic patches or thin plaques with fine-scale Color varies from pink to red-brown +/- epidermal atrophy/poikiloderma (large plaque parapsoriasis).

26
Q

Age distribution for small plaque parapsoriasis?

A

Peaks during 5th decade

27
Q

Sex differences in small plaque parapsoriasis?

A

M:F 3:1

28
Q

What are the plaques made up of in small plaque parapsoriasis?

A

Superficial cutaneous lymphoid infiltrates composed primarily of CD4+ T-cells.

29
Q

What is the histology of small-plaque parapsoriasis?

A

Mild non-specific spongiotic dermatitis with focal parakeratosis, +/- exocytosis of lymphocytes

30
Q

The difference in pathophysiology between small and large plaque parapsoriasis?

A

Dominant T-cell clonality is seen in pt’s with large plaque parapsoriasis. In some cases, it may actually be patch stage mycosis fungoides.

31
Q

What form of large-plaque parapsoriasis virtually always progresses to mycosis fungoides?

A

Retiform varients (rare)

32
Q

Progression of large plaque parapsoriasis to more overt forms of lymphoma?

A

10-35% over 6-10 years.

33
Q

Tx for small plaque parapsoriasis?

A

Topical CS, calcineurin inhibitors, coal, light therapy, topical bexarotene, imiquimod. If there is itching then you can use antihistamines.

34
Q

Difference clinically between PLEVA and PLC lesions?

A

PLEVA lesions are crusted and occasionally vesiculpustular whereas in PLC they are scaly

35
Q

Pt hx of PLEVA/PLC?

A

Recurrent crops of spontaneously regressing erythematous papules. This is important as PR will have the herald patch and then all the lesions will go away, you wont get recurrent lesions nearly as commonly.

36
Q

What is the difference in T-cell infiltrates in PLEVA vs PLC?

A

PLEVA = CD8+ t-cell predominance, PLC = CD4+ predominance

37
Q

What can trigger PLEVA/PLC?

A

Infx: HIV, parovirus B19 Drugs: estrogen-progesterone, TNF-a inhibitors (infliximab and adalimumab), statins, radiocontrast dye low-grade T-cell lymphoproliferative dz.

38
Q

What type of dz is PLEVA often considered?

A

T-cell lymphoproliferative diosrder (more so than PLC) as there is more t-cell clonality in PLEVA as compared to PLC

39
Q

Key clinical findings in PLEVA?

A

Rapid onset of widespread (trunk, buttocks, proximal extremities> other sites) pink papules that evolve into vesicular, ulceronecrotic, purpuric, and crusted papules which then heal with varioliform scars after weeks

40
Q

What is Mucha-Haberman dz?

A

This is PLEVA but with high fevers, consitutional sx’s, LAD, arthritis, mucosal involvement, pulmonary involvement, and GI involvement. (increased TNF-a levels)

41
Q

Clinical findings of PLC?

A

Widespread, scaly, red-brown, papules and plaques Resolves with hypopigmentation after weeks to months (longer than PLEVA) Adults: PLC > PLEVA More diffuse distribution= shortest disease course (avg 11 months) Limited/peripheral distribution= longest disease course (avg 33 months)

42
Q

Clinical progression of PRP?

A

Begins on the head/neck and progresses caudally

43
Q

Nail findings in PRP?

A

Thick yellow-brown nails w/ subungal debris; no nail pits like psoriasis.

44
Q

Tx for PRP?

A

Isotretinoin (unlike psoriasis), acitretin, high dose vit A, MTX, TNFa inhibitors, phototherapy

45
Q

What are the genetic findings in Type V PRP (atypical juvenile)

A

Heterozygous gain of function mutation in CARD1 aka PSOR2 psoriasis susceptibility gene

46
Q

What is the “Wong type” of PRP eruption?

A

PRP eruptions seen in pt’s with dermatomyositis

47
Q

Describe Type I PRP

A

Classic PRP in adult. spreads caudally, red-orange plaques w/ islands of sparing, perifollicular keratotic papules, waxy palmoplantar keratoderma.

most clears within 3 yrs
represents 55% of PRP

48
Q

Describe Type II PRP

A

Adults, areas of eczematous dermatitis, ichythyosiform scale on legs, keratoderma w/ coarse lamellated scale, occasional alopecia

Chronic course
5% of PRP

49
Q

Describe type III PRP

A

Classic Juvenile Findings seen in type I, peak onset is first 2 yrs of life and adolescence.

clears in 3 years
10% of PRP

50
Q

Describe type IV PRP

A

Focal Juvenile PRP -M/c on the elbows and knees, erythema, follicular papules, prepubertal onset.

variable course
25% of PRP

51
Q

Describe type V PRP

A

Atypical Juvenile Follicular hyperkeratosis, erythema, scleroderma-like changes of hands and feet, accounts for most familial cases of PRP w/ mutations in CARD1 (PSOR2), onset in the first few years of life

chronic course
5% of PRP

52
Q

Describe type VI PRP

A

HIV associated PRP -overalp w/ type I -other findings = follicular spines, acne conglobata, HS

most rare form= <1%

53
Q

What is granular parakeratosis

A

Primary lesions are brownish-red keratotis papules that can coalesce into plaques. Adult form is almost exclusvely in women. Most cases are in the axillae but can be in other intertrigineous sites too.

infantile form is a/w diaper wearing and can be b/l plaques in inguinal folds or erythematous geometric plaques under pressure points from diaper.

54
Q

Histopathology of granular parakeratosis?

A

This is really the key to the name, there is distinct retention of the keratohyalin granules in the parakeratosis.

55
Q

Tx for granular parakeratosis?

A

topical: corticosteroids, vitamin D analogs, keratolytics, and antifungals,

destructive: cryotherapy, systemic: isotretinoin, antifungals

DERM (03) Papulosquamous Disease (4 decks)

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